miR‑204‑5p promotes apoptosis and inhibits migration of gastric cancer cells by targeting HER‑2

miR-204-5p通过靶向HER-2促进胃癌细胞凋亡并抑制迁移

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作者:Shu Yang, Binni Chen, Baogen Zhang, Caiping Li, Yuena Qiu, Hanhui Yang, Zhongxin Huang

Abstract

Gastric cancer is one of the most common types of cancer worldwide, with a high incidence and mortality rate. MicroRNAs (miRs) play an important role in tumorigenesis, cell proliferation, migration, apoptosis and metastasis of cancer. The present study aimed to investigate the role and potential mechanism of miR‑204‑5p in gastric cancer. The mRNA expression levels of miR‑204‑5p in gastric cancer were determined by reverse transcription‑quantitative PCR. Cell proliferation was determined using Cell Counting Kit‑8 and colony formation assays. Flow cytometry analysis was performed to detect the cell apoptosis rate. Wound healing and Transwell assays were carried out to determine the cell migration and invasion rates, respectively. A putative binding site of miR‑204‑5p in the 3' untranslated region of human epidermal growth factor receptor 2 (HER‑2) was predicted using a bioinformatics algorithm and confirmed using a dual‑luciferase reporter assay. miR‑204‑5p levels were downregulated in gastric cancer cells. Overexpression of miR‑204‑5p significantly inhibited cell proliferation and decreased cell colony formation. Additionally, miR‑204‑5p decreased the migration and invasion rates of gastric cancer cells. Furthermore, an increased apoptotic rate was detected following overexpression of miR‑204‑5p, along with increased expression levels of Bax and decreased expression levels of Bcl‑2. HER‑2 was a direct target of miR‑204‑5p, and inhibition of HER‑2 acted as a tumor suppressor by inhibiting cell proliferation, migration and invasion, and promoting cell apoptosis, which was reversed by the inhibition of miR‑204‑5p expression. These results suggested that miR‑204‑5p could exert its anti‑tumor function by inhibiting cell proliferation, migration and invasion, and promoting cell apoptosis via regulation of HER‑2, which may be a potential therapeutic target for gastric cancer.

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